Compound Monograph
Kaempferitrin
Kaempferitrin is kaempferol-3,7-O-α-L-dirhamnoside (synonym lespedin) — a flavonol diglycoside of epazote, Justicia and many plants. No human trial of the isolate exists; its evidence is a small preclinical set led by a genuine insulin-mimetic antidiabetic signal (it stimulates glucose uptake in skeletal muscle and is hypoglycemic in diabetic rodents), with anti-inflammatory and antioxidant data. Poorly absorbed and hydrolyzed toward kaempferol in the gut.
Sources · 5
Where Does It Come From?
Kaempferitrin is a naturally occurring flavonol glycoside (kaempferol-3,7-o-α-l-dirhamnoside), found in Epazote and 4 other sources. It is well tolerated orally (low toxicity).
Concentration
Content by Source
Concentrations not reported. No percent-dry-weight or mg/g figures have been published for this compound in its source plants.
Kaempferitrin at a Glance
Kaempferitrin is kaempferol-3,7-O-alpha-L-dirhamnoside — a flavonol diglycoside of epazote, Justicia and many other plants, also known as lespedin.
Its evidence is a small preclinical set led by a genuinely notable finding: insulin-like hypoglycaemic activity, reported to lower blood glucose in diabetic animals with a rapidity more typical of a hormone than a flavonoid.
No human trial of the isolate exists.
What It's Used For
Kaempferitrin is the 3,7-dirhamnoside of kaempferol (synonym lespedin, an identity established in 1951 13Reference 13Identity of lespedin with kaempferitrinView study →) — a sibling of the monoglucoside astragalin, from which it differs by carrying a second (7-position) sugar and swapping glucose for rhamnose (twice). Its evidence is a small, multi-lab preclinical literature clustered on one genuinely distinctive signal: an insulin-mimetic antidiabetic effect. Unlike most flavonol glycosides, kaempferitrin shows an intact-molecule action in muscle — so it is not purely a kaempferol prodrug — although its poor absorption and gut-flora hydrolysis toward kaempferol still make chronic oral benefit bioavailability-limited. No human trials of the isolate exist.
Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. No human isolate data, so scores stay low by design.
The most-developed and most kaempferitrin-specific activity. Kaempferitrin acutely stimulates ¹⁴C-glucose uptake in rat soleus (skeletal) muscle in an insulin-mimetic, insulin-signaling-dependent manner 1Reference 1AnimalInsulinomimetic effects of kaempferitrin on glycaemia and on ¹⁴C-glucose uptake in rat soleus muscleView study →, activates insulin signaling and adiponectin secretion in adipocytes 3Reference 3Kaempferitrin activates the insulin signalling pathway and stimulates secretion of adiponectin in 3T3-L1 adipocytesView study →, drives glucose uptake in skeletal muscle 5Reference 5Insulin signalling: a potential pathway for the stimulatory effect of kaempferitrin on glucose uptake in skeletal muscleView study →, and in mice modulated hepatic AMPK phosphorylation and lowered PEPCK (gluconeogenesis) after a high-fat/high-sucrose diet 6Reference 6AnimalKaempferitrin modulates AMPK phosphorylation and PEPCK expression in the liver after a short-term high-fat, high-sucrose diet in miceView study →.
The classic in-vivo anchor is a hypoglycemic + antioxidant effect in diabetic rats for the isolated dirhamnoside from Bauhinia forficata 2Reference 2Hypoglycemic effect and antioxidant potential of kaempferol-3,7-O-(α)-dirhamnoside from Bauhinia forficata leavesView study →.
Gap: all preclinical, and tissue-divergent — one adipocyte study reports kaempferitrin inhibits GLUT4 translocation and glucose uptake 4Reference 4Kaempferitrin inhibits GLUT4 translocation and glucose uptake in 3T3-L1 adipocytesView study →, conflicting with the muscle picture, with no standardized dose-response and no human trial 1,
Kaempferitrin shows consistent NF-κB restraint across unrelated models: it attenuated LPS-induced septic acute lung injury 7Reference 7AnimalKaempferitrin alleviates LPS-induced septic acute lung injury in mice through downregulating the NF-κB pathwayView study →, inhibited proliferation and inflammation in rheumatoid-arthritis synoviocytes 8Reference 8Kaempferitrin inhibits proliferation, induces apoptosis and ameliorates inflammation in rheumatoid-arthritis fibroblast-like synoviocytesView study →, and reduced renal inflammation and fibrosis by inhibiting NOX4-mediated tubular ferroptosis 9Reference 9Kaempferitrin attenuates unilateral-ureteral-obstruction-induced renal inflammation and fibrosis by inhibiting NOX4-mediated tubular ferroptosisView study →.
Gap: three single-model rodent/cell studies, with no replication or human data, largely shared with the kaempferol/flavonol class 7,
Kaempferitrin’s antioxidant activity overlaps its antidiabetic story: radical scavenging linked to hypoglycemia in diabetic rats 2Reference 2Hypoglycemic effect and antioxidant potential of kaempferol-3,7-O-(α)-dirhamnoside from Bauhinia forficata leavesView study → and protection of mesangial cells from advanced-glycation-end-product-induced apoptosis and oxidative stress 14Reference 14Protective effects of kaempferitrin on advanced-glycation-end-product-induced mesangial-cell apoptosis and oxidative stressView study →.
Gap: class-level flavonol antioxidant behavior in narrow models, not distinctively kaempferitrin 2,
Kaempferitrin induces intrinsic apoptosis in HeLa cells 10Reference 10Kaempferitrin induces apoptosis via the intrinsic pathway in HeLa cellsView study →, and as the major compound of an epazote ethanol extract it produced antitumor and hepatoprotective effects in a human-liver-cancer mouse xenograft without hepatotoxicity 11Reference 11AnimalKaempferitrin, a major compound from the ethanol extract of Chenopodium ambrosioides (epazote), exerts antitumour and hepatoprotective effects in mice with human liver-cancer xenograftsView study →.
Gap: heterogeneous and exploratory — single studies at the isolate or extract level, with no translational follow-up 10,
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| Skeletal-muscle glucose uptake (insulin-mimetic) | ↑ uptake, insulin-signaling-dependent | antidiabetic |
| Insulin signaling (IR → PI3K/Akt) + adiponectin | pathway activated; ↑ adiponectin | antidiabetic |
| GLUT4 translocation | tissue-divergent — muscle uptake up, but inhibited in one adipocyte study | antidiabetic (nuance/contradiction) |
| Hepatic AMPK / PEPCK | ↑ AMPK, ↓ PEPCK → ↓ gluconeogenesis | antidiabetic (in vivo) |
| NF-κB; NOX4 → tubular ferroptosis | suppressed; inhibited | anti-inflammatory / antioxidant |
| ROS / AGE-induced oxidative stress | reduced | diabetic-complication protection |
| Intrinsic (mitochondrial) apoptosis | pro-apoptotic in tumor cells | antitumor |
Pharmacokinetics
No dedicated human pharmacokinetics exists. As a flavonol 3,7-di-O-rhamnoside, kaempferitrin is a poorly absorbed, high-polarity diglycoside: the two rhamnose units block passive uptake, and human intestinal flora biotransform it by stepwize deglycosylation (loss of rhamnose → monorhamnoside intermediates → the aglycone kaempferol), which is then conjugated 12Reference 12The biotransformation of kaempferitrin by human intestinal floraView study →. The net result is low, non-sustained systemic exposure to the intact parent, and a meaningful fraction of chronic in-vivo activity should be read as kaempferol-equivalent exposure (see kaempferol). The important nuance: the acute insulin-mimetic muscle effects are reported for the intact molecule in ex-vivo/cell systems, so the antidiabetic mechanism is not purely a kaempferol proxy — but oral, whole-animal benefit is bioavailability-limited.
Clinical trials
There are no randomized or open-label human trials of isolated kaempferitrin for any indication; human relevance is limited to dietary/traditional intake within kaempferitrin-bearing plants (epazote, Justicia spicigera, Bauhinia forficata).
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| —(none, isolate) | — | — | Small multi-lab set (antidiabetic-led) |
Last checked: July 2026.
Toxicity & Safety
Kaempferitrin is a dietary flavonol glycoside with no harm signal at food levels, and the only caution with a real mechanism behind it is the mirror image of its main effect — its glucose-lowering activity could add to antidiabetic medication.
- A dietary flavonol with no harm signal. Used across preclinical studies as a protective agent; one extract study reported antitumor efficacy without hepatotoxicity.
- Avoid isolated supplements in pregnancy and lactation. Dietary amounts are a separate question.
- Possible additive hypoglycemia. The insulin-mimetic signal makes stacking with antidiabetic drugs plausible in theory, though unquantified in humans.
- Generic polyphenol-supplement caution. Possible additive effects with antiplatelet or anticoagulant therapy.
- No isolate toxicology. No genotoxicity or human safety dataset exists for the purified compound.
Full Safety & Interactions Detail
Kaempferitrin is a dietary flavonol glycoside in food and medicinal plants, used across preclinical studies as a protective or benign agent with no dietary harm signal — consistent with a low flag; notably, the epazote-extract xenograft study reported antitumor efficacy without hepatotoxicity 11Reference 11AnimalKaempferitrin, a major compound from the ethanol extract of Chenopodium ambrosioides (epazote), exerts antitumour and hepatoprotective effects in mice with human liver-cancer xenograftsView study →.
There is no isolate toxicology, genotoxicity or human safety dataset, and cautions are theoretical and generic to concentrated polyphenol supplements (possible additive effects with antiplatelet/anticoagulant therapy). One specific pharmacodynamic caution: given the insulin-mimetic/glucose-lowering signal, additive hypoglycemia with antidiabetic drugs is plausible in theory though unquantified in humans.
Dosage
There is no efficacy dose established (no human trials) and no standard supplemental dose — kaempferitrin is obtained incidentally through diet and herbal preparations rather than dosed on its own, and any oral efficacy target is undercut by its poor absorption and gut-flora hydrolysis to kaempferol, so a meaningful “kaempferitrin dose” cannot honestly be stated.
References
- Jorge AP, Horst H, de Sousa E, et al. (2004). Insulinomimetic effects of kaempferitrin on glycaemia and on ¹⁴C-glucose uptake in rat soleus muscle. Chemico-Biological Interactions. https://pubmed.ncbi.nlm.nih.gov/15501431/
- de Sousa E, Zanatta L, Seifriz I, et al. (2004). Hypoglycemic effect and antioxidant potential of kaempferol-3,7-O-(α)-dirhamnoside from Bauhinia forficata leaves. Journal of Natural Products. https://pubmed.ncbi.nlm.nih.gov/15165145/
- Tzeng YM, Chen K, Rao YK, et al. (2009). Kaempferitrin activates the insulin signalling pathway and stimulates secretion of adiponectin in 3T3-L1 adipocytes. European Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/19326566/
- Vishnu Prasad CN, Suma Mohan S, Banerji A, et al. (2009). Kaempferitrin inhibits GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes. Biochemical and Biophysical Research Communications. https://pubmed.ncbi.nlm.nih.gov/19146827/
- Cazarolli LH, Pereira DF, Kappel VD, et al. (2013). Insulin signalling: a potential pathway for the stimulatory effect of kaempferitrin on glucose uptake in skeletal muscle. European Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/23458067/
- Garofolo IC, Santos PF, Silva MF, et al. (2026). Kaempferitrin modulates AMPK phosphorylation and PEPCK expression in the liver after a short-term high-fat, high-sucrose diet in mice. Nutrition and Health. https://pubmed.ncbi.nlm.nih.gov/40390681/
- Zhu X, Pan Y, Xu X, et al. (2023). Kaempferitrin alleviates LPS-induced septic acute lung injury in mice through downregulating the NF-κB pathway. Allergologia et Immunopathologia. https://pubmed.ncbi.nlm.nih.gov/37937489/
- Wang J, Zhao Q (2019). Kaempferitrin inhibits proliferation, induces apoptosis and ameliorates inflammation in rheumatoid-arthritis fibroblast-like synoviocytes. Phytotherapy Research. https://pubmed.ncbi.nlm.nih.gov/31155798/
- Li J, Yang J, Xian Q, et al. (2024). Kaempferitrin attenuates unilateral-ureteral-obstruction-induced renal inflammation and fibrosis by inhibiting NOX4-mediated tubular ferroptosis. Phytotherapy Research. https://pubmed.ncbi.nlm.nih.gov/38487990/
- Alonso-Castro AJ, Ortiz-Sánchez E, García-Regalado A, et al. (2013). Kaempferitrin induces apoptosis via the intrinsic pathway in HeLa cells. Journal of Ethnopharmacology. https://pubmed.ncbi.nlm.nih.gov/23211658/
- Su M, Li Z, Zhou S, et al. (2023). Kaempferitrin, a major compound from the ethanol extract of Chenopodium ambrosioides (epazote), exerts antitumour and hepatoprotective effects in mice with human liver-cancer xenografts. Journal of Pharmacy and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/37203217/
- Yang XW, Zhang JY, Xu W, et al. (2005). The biotransformation of kaempferitrin by human intestinal flora. Acta Pharmaceutica Sinica. https://pubmed.ncbi.nlm.nih.gov/16268506/
- HATTORI S (1951). Identity of lespedin with kaempferitrin. Nature. https://pubmed.ncbi.nlm.nih.gov/14882347/
- Jiang W, Wang R, Liu D, et al. (2018). Protective effects of kaempferitrin on advanced-glycation-end-product-induced mesangial-cell apoptosis and oxidative stress. International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/30373106/
